Thrombophilia in patients with chronic venous leg ulcers-a study on patients with or without post-thrombotic syndrome

被引:11
|
作者
Zutt, M. [1 ]
Krueger, U. [1 ]
Rosenberger, A. [2 ]
Schoen, M. P. [1 ]
Neumann, C. [1 ]
von Ahsen, N. [3 ]
Kretschmer, L. [1 ]
机构
[1] Univ Gottingen, Dept Dermatol Venereol & Allergol, Gottingen, Germany
[2] Univ Gottingen, Sch Med, Dept Genet Epidemiol, Gottingen, Germany
[3] Univ Gottingen, Dept Clin Chem, Gottingen, Germany
关键词
ACTIVATED PROTEIN-C; FACTOR-V-LEIDEN; RISK-FACTORS; ANTIPHOSPHOLIPID ANTIBODIES; REDUCTASE C677T; PLASMA-LEVELS; PREVALENCE; RESISTANCE; HYPERHOMOCYSTEINEMIA; DEFICIENCY;
D O I
10.1111/j.1468-3083.2011.04001.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Background Chronic venous leg ulcers (CVU) cause considerable burden of disease for the patients as well as enormous costs for health care systems. The pathophysiology of CVU is complex and not entirely understood. So far reliable pathogenic and/or prognostic parameters have not been identified. Objectives We studied the role of thrombophilia in patients referred to a University dermatology department for treatment of CVU. Patients and methods A cohort of 310 patients with active chronic venous leg ulcers (CEAP 6) was stratified into two comparably large groups according to the presence or absence of post- thrombotic syndrome (PTS+; PTS-) as determined using duplex scan and/or phlebography. In addition, several thrombophilia parameters were assessed. Results The prevalence of protein S deficiency and factor V Leiden mutation was significantly higher in PTS+ patients compared with the PTS- group. However, patients in both subgroups revealed high prevalences of thrombophilia (antithrombin deficiency, protein C deficiency, protein S deficiency, activated protein C resistance, factor V mutation or elevated homocysteine). Conclusion Based on these data, it is conceivable that thrombophilia contributes to the pathogenesis of CVU, possibly through induction of microcirculatory dysregulations.
引用
收藏
页码:1432 / 1439
页数:8
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